Involvement of oxidative stress induction in Na+ toxicity and its relation to the inhibition of a Ca2+ -dependent but calcineurin-independent mechanism in Saccharomyces cerevisiae

J Biosci Bioeng. 2006 Jan;101(1):77-9. doi: 10.1263/jbb.101.77.

Abstract

Uridine 5'-hexadecylphosphate (UMPC16) inhibited the growth of Saccharomyces cerevisiae under a hypersaline stress condition with Na+ more strongly than the calcineurin inhibitor cyclosporine A (CsA). Additional Ca2+ supplementation similarly suppressed the inhibitory activities of UMPC16 and CsA on yeast cell growth in a medium with Na+. UMPC16, but not CsA, accelerated mitochondrial reactive oxygen species (ROS) generation in combination with Na+, suggesting its inhibition of a Ca2+ -dependent but calcineurin-independent mechanism for protection against Na+ toxicity.

MeSH terms

  • Calcineurin Inhibitors
  • Calcium / pharmacology*
  • Cyclosporine / antagonists & inhibitors
  • Cyclosporine / pharmacology
  • Mitochondria / metabolism
  • Osmotic Pressure
  • Oxidative Stress* / drug effects
  • Reactive Oxygen Species / metabolism
  • Saccharomyces cerevisiae / drug effects*
  • Saccharomyces cerevisiae / physiology*
  • Sodium / antagonists & inhibitors
  • Sodium / toxicity*
  • Uridine Monophosphate / analogs & derivatives
  • Uridine Monophosphate / antagonists & inhibitors
  • Uridine Monophosphate / pharmacology

Substances

  • Calcineurin Inhibitors
  • Reactive Oxygen Species
  • uridine 5'-hexadecylphosphate
  • Cyclosporine
  • Sodium
  • Uridine Monophosphate
  • Calcium